Alcoholic Ketoacidosis: Mind the Gap, Give Patients What They Need EMRA

Triglycerides stored in adipose tissue undergo lipolysis and are released into the circulation as free fatty acids bound ionically to albumin. Free fatty acids are removed by the liver, where they primarily undergo oxidation to hydroxybutyric acid and acetoacetate and subsequently are reesterified to triglyceride. Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can increase the rate of ketogenesis. Alcoholic ketoacidosis (AKA) is a complex metabolic condition. It’s helpful to know a little bit about how the body works to understand this condition.

The resulting increase in the NADH/NAD+ ratio inhibits hepatic gluconeogenesis and elevates the ratio of hydroxybutyric acid to acetoacetic acid. Acetic acid (an acyl group carrier) is linked with coenzyme A (a https://ecosoberhouse.com/article/alcoholic-ketoacidosis-symptoms-and-treatment/ thiol) to produce Acetyl-CoA. This process is catalyzed by the enzyme acetyl-CoA synthetase. Intravenous benzodiazepines can be administered based on the risk of seizures from impending alcohol withdrawal.

Inhaled industrial acetylene: A diabetic ketoacidosis mimic

The dextrose will also increase glycogen stores and diminish counterregulatory hormone levels. It is essential to administer thiamine before any glucose administration to avoid Wernicke’s encephalopathy preci[itation. If severe hypokalemia is present dextrose containing fluids can be held until potassium levels are normalized. Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia. Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. The reversal of ketosis and vigorous rehydration are central in the management of AKA.

In contrast to diabetic ketoacidosis, the predominant ketone body in AKA is β-OH. Routine clinical assays for ketonemia test for AcAc and acetone but not for β-OH. Clinicians underestimate the degree of ketonemia if they rely solely on the results of laboratory testing.

Signs and symptoms

In general, the prognosis for a patient presenting with AKA is good as long as the condition is identified and treated early. The major cause of morbidity and mortality in patients diagnosed with AKA is under-recognition of concomitant diseases (that may have precipitated the AKA, to begin with). These include acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal. Mortality specifically due to AKA has been linked to the severity of serum beta-hydroxybutyric acid in some studies. It should be used as an indicator of the severity of the disease.[13] Identifying these high-risk patients can help set the intensity of monitoring required for the patient to ensure optimal patient outcomes are achieved. Twenty-four chronic alcohol abusers hospitalized during a twenty-seven-month period were suspected of having “alcoholic ketoacidosis” because they had ketonuria or ketonemia with little or no glucosuria.

Initial IV fluids should contain added water-soluble vitamins and magnesium, with potassium replacement as required. Most cases of AKA occur when a person with poor nutritional status due to long-standing alcohol abuse who has been on a drinking binge suddenly decreases energy intake because of abdominal pain, nausea, or vomiting. In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis. Most patients had eaten poorly for several days (and usually longer) and had allegedly decreased their alcohol intake during that period. That history, and the usual rapid clearing of ketosis simply by treatment with solutions of glucose and NaCl, suggested that acute starvation was an important factor in the pathogenesis of this disorder. If you or someone you know has an alcohol use disorder, they may be at risk of developing alcoholic ketoacidosis.

Management

If not treated quickly, alcoholic ketoacidosis may be life-threatening. The absence of hyperglycemia makes diabetic ketoacidosis improbable. Those with mild hyperglycemia may have underlying diabetes mellitus Diabetes Mellitus (DM) Diabetes mellitus is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia. Early symptoms are related to hyperglycemia and include polydipsia…

If you have symptoms of alcoholic ketoacidosis, your doctor will perform a physical examination. They will also ask about your health history and alcohol consumption. If your doctor suspects that you’ve developed this condition, they may order additional tests to rule out other possible conditions.